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anti-Mouse (Murine) NFKBIE Antibodies:
anti-Human NFKBIE Antibodies:
anti-Rat (Rattus) NFKBIE Antibodies:
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The basic residues Lys (show LYZ Antibodies)-717 and Lys (show LYZ Antibodies)-719 in the C-terminal region of ANK7 contribute to IkappaBzeta (show NFKBIZ Antibodies) binding to the Lcn2 (show LCN2 Antibodies) promoter, probably via interaction with the cytosine-rich element required for Lcn2 (show LCN2 Antibodies) activation; glutamate (show GRIN1 Antibodies) substitution for both lysines results in a loss of transcriptionally active complex formation without affecting direct contact of IkappaBzeta (show NFKBIZ Antibodies) with p50 (show LSP1 Antibodies).
The data imply that regulation of these c-Rel (show NFkBP65 Antibodies)-dependent lymphoid responses is a non-redundant function of IkappaBepsilon.
temporal control of NF-kappaB (show NFKB1 Antibodies) activation by the coordinated degradation and synthesis of IkappaB proteins
IkappaBepsilon deficiency in mice leads to neonatal death, elevated kappaB binding activity, overexpression of NF-kappaB (show NFKB1 Antibodies) target genes, and disruption of lymphocyte production.
Neither IkappaBalpha (show NFKBIA Antibodies) nor IkappaBepsilon deficiency had major effects on natural killer cell generation while their combined absence led to NF-kappaB (show NFKB1 Antibodies) hyperactivation.
An important role is proposed for I kappa B epsilon in the differential regulation of nuclear NF-kappa B (show NFKB1 Antibodies) activity in stimulated B cells.
In vivo degradation rate constants were measured for NF-kappaB (show NFKB1 Antibodies)-bound & -unbound IkappaB. Models suggest differential degradation rates of free & bound IkappaB may be a new cross-regulation mechanism imparting functional robustness to the signaling module.
identify NFKBIE aberrations as a common genetic event across B-cell malignancies and highlight NFKBIE deletions as a novel poor-prognostic marker in PMBL.
We suggest that the impairment of NFKBIE gene function can reduce the uptake of methotrexate into cells, suggesting that the gene is an important factor for rheumatoid arthritis outcome
A NFKBIE polymorphism was associated with increased risk of pneumococcal meningitis.
results show that Gal-1 (show LGALS1 Antibodies) acts by inhibiting the stimulation of the LPS (show IRF6 Antibodies)-induced IkappaBzeta (show NFKBIZ Antibodies) expression, an NF-kappaB (show NFKB1 Antibodies) regulator involved in IL-6 (show IL6 Antibodies) gene transcription.
Newly identified alterations included recurrent promoter mutations of NFKBIE, encoding NF-kappaB (show NFKB1 Antibodies) inhibitor varepsilon (IkappaBvarepsilon), in 14.5% of samples of desmoplastic melanoma
IkappaBepsilon has a role in NF-kappaB (show NFKB1 Antibodies) regulation in aggressive chronic lymphocytic leukemia
Vitamin C forestalls cigarette smoke induced NF-kappaB (show NFKB1 Antibodies) activation in alveolar epithelial cells.
we identified two gene loci associated with rheumatoid arthritis susceptibility- NFKBIE and RTKN2 (show RTKN2 Antibodies)
Protein phosphatase 6 subunit with conserved Sit4-associated protein domain targets IkappaBepsilon
An NFKBIE SNP associated with susceptibility to pneumococcal disease but not pneumococcal empyema.
The protein encoded by this gene binds to components of NF-kappa-B, trapping the complex in the cytoplasm and preventing it from activating genes in the nucleus. Phosphorylation of the encoded protein targets it for destruction by the ubiquitin pathway, which activates NF-kappa-B by making it available to translocate to the nucleus.
nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon
, NF-kappa-B inhibitor epsilon
, solute carrier family 35, member B2